High Velocity Nasal Insufflation (Hi-VNI) Used to Avoid NIV and Reverse Acute Carbon Dioxide Retention in a COPD Exacerbation

Vapotherm’s Hi-VNI Technology is a tool for treating the signs and symptoms of respiratory distress. The enclosed materials describe certain outcomes in relation to the use of Vapotherm’s Hi-VNI Technology, but individual results may vary. Practitioners should refer to the full indications for use and operating instructions of any products referenced herein before prescribing them.

Patient History and Presentation
A 60 year-old female with a history of end-stage COPD, having been intubated within the last month for a similar exacerbation, arrived by ambulance to our Emergency Department. The chief complaint was severe difficulty breathing which came on gradually. Initial assessment noted tachypnea with nasal flaring and purse lipped breathing, as well as bilateral wheezing and wet cough.

This patient is well known to our staff with multiple prior admissions. Eighteen days prior, this patient presented with a similar exacerbation, wherein she was intubated and admitted to the ICU with a three day length of stay. Based on history, it was anticipated that this patient would be intubated and admitted to the ICU.

Treatment and Response
Non-Invasive ventilation was ordered but never initiated; Hi-VNI was started (Precision Flow, Vapotherm, Exeter, NH: Adult cannula with 4.8mm O.D.) at 25 L/min with a 60% oxygen blend and the patient immediately and markedly began to improve. Arterial blood gas analyses (ABGs) were made immediate after the initiation of Hi-VNI, and again 44 minutes thereafter; data are reported below. Following the initiation of Hi-VNI, respiratory rate dropped precipitously and the patient demonstrated a reduction in dyspnea. In the time between ABGs, and despite the drop in respiratory rate, PaCO2 was reduced and pH increases markedly. Arterial oxygen tension dropped in conjunction with the decrease in respiratory rate, but hemoglobin oxygen saturation was maintained. The patient was admitted to the medical floor and discharged the following day.

Interpretation
In conjunction with the mechanistic evidence that Hi-VNI provides ventilation support by way of dead space purge, Hi-VNI resulted in a reduced minute ventilation by way of a reduction in respiratory rate. The blow-off of CO2 from the anatomical dead space improved arterial CO2, and corresponding pH, despite the drop in rate. The improvement in pH stabilized hemoglobin saturation in the face of a reduced arterial oxygen tension (Bohr effect) that was associated with the drop in minute ventilation. The arterial CO2 was reduced to 53 mmHg, which is normal for a compensated COPD patient (HCO3– = 33 mEq/L), and so much of the ventilation work was seen as a reduced respiratory rate. This reduced work of breathing likely averted respiratory muscle fatigue.

Conclusions
The application of Hi-VNI resulted in rapid improvement that is believed to have averted the use of mechanical ventilation and ICU admission. Note that this patient returned twelve days later with an identical presentation, and was again successfully treated with Hi-VNI.